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Serum Lactate as a Marker of Acute Myocardial Infarction



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Am Fam Physician. 1998 Apr 15;57(8):1993-1994.

Five million patients visit emergency departments annually with a chief complaint of chest pain, although fewer than 15 percent are diagnosed with acute myocardial infarction. Early diagnosis of acute myocardial infarction in patients with acute onset of chest pain continues to be a problem. Information obtained on presentation, such as the patient's clinical history, baseline vital signs and initial electrocardiogram (ECG) readings, is often unreliable, and rapid assays of creatine phosphokinase (CK), CK-MB subforms, and troponin T and troponin I may not rise for six to 12 hours. Serum lactate, however, is a well established marker of inadequate systemic perfusion and resulting tissue hypoxia. Schmiechen and associates evaluated the question of whether serum lactate levels could be used to confirm a diagnosis of acute myocardial infarction or other acute illness in patients with acute chest pain.

All patients aged 18 years and older who visited the emergency department within 24 hours of experiencing chest pain or other cardiac symptoms were eligible for inclusion in the study. On presentation, blood samples were obtained to evaluate serum lactate levels. A positive lactate finding was defined as a blood lactate concentration of 13.5 mg per dL (1.5 mmol per L) or greater. In addition, serial CK and CK-MB levels and ECG readings were obtained, along with standard vital signs and a medical history, which were used by physicians in the cardiology department to make the diagnosis of acute myocardial infarction.

Of the 129 patients who were included in the study, 28 had a documented acute myocardial infarction. The mean patient age was 58 years, and the ratio of men to women was 1.6:1. All but one of the patients with acute myocardial infarction had a positive serum lactate finding. Of the 101 patients in the group without acute myocardial infarction, 46 had positive serum lactate levels. The overall sensitivity of a positive lactate finding for acute myocardial infarction was 96 percent, and the specificity was 55 percent. This yields a negative predictive value of 98 percent and a positive predictive value of 37 percent. Fourteen of the patients with acute myocardial infarction had normal CK and CK-MB values at the time of admission; however, the CK-MB levels eventually increased in all of these patients. Vital signs did not significantly differ in either group.

The authors conclude that, unlike adjuncts typically used to diagnose acute myocardial infarction, serum lactate levels measured within three hours of the onset of symptoms are highly sensitive for acute myocardial infarction, significantly more so than CK and CK-MB levels measured at that time. The level of serum lactate is thought to rise rapidly in patients with acute myocardial infarction because of poor systemic perfusion secondary to uncompensated cardiac ischemia. However, the low specificity of lactate means that it should not be used in place of CK and CK-MB determinations to direct thrombolytic therapy. Hyperlactemia also appears to correlate with critical illness and mortality in patients presenting with chest pain. The authors note that the use of lactate levels may be limited, since conditions such as renal insufficiency, smoke inhalation, seizures and alcohol intoxication tend to cause unreliably elevated lactate levels. However, patients with normal lactate levels, medical history and ECG findings could be considered at low risk for acute myocardial infarction and may benefit from this quick, simple, inexpensive “rule out” test.

Schmiechen NJ, et al. ED use of rapid lactate to evaluate patients with acute chest pain. Ann Emerg Med. 1997 November;30:571–7.


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